Left ventricular thrombus (LVT) is associated with a significant risk of ischemic stroke (IS) and peripheral embolization. Societal guidelines recommend the use of warfarin, with direct oral anticoagulants (DOACs) only for patients unable to tolerate warfarin. We studied the natural history of LVT with anticoagulation (AC) with emphasis on comparing warfarin and DOAC use. In this single center study, we identified patients with a confirmed LVT. Type and duration of anticoagulation, INR levels and clinical outcomes (bleeding, ischemic stroke or peripheral embolization, and thrombus resolution) were recorded. LVT was confirmed in a total of 110 patients. Mean age was 59 + 14 years. 79% were men. Underlying etiology was chronic ischemic cardiomyopathy in 58%, non-ischemic cardiomyopathy in 23%. AC was started in 96 (87%) patients. At 1 year follow up, 11 patients (10%) had a stroke while on any AC (2 had hemorrhagic stroke and 9 had IS). Of those with IS, 7 were on warfarin (71% of those had subtherapeutic INR) and 2 patients on DOACs had IS. The 1-year risk of any stroke was 15% in warfarin group (12% risk of ischemic stroke) compared to 6% in the DOACs group (p = 0.33). 37 (63%) patients on warfarin and 18 (53%) on DOACs had resolution of thrombus (p = 0.85). One-year risk of stroke with LVT is high (10%) even with AC. Most patients IS on warfarin had subtherapeutic INR. There was no statistical difference in stroke risk or rate of thrombus resolution between warfarin and DOACs treated patients.

Hydroxychloroquine, initially used as an antimalarial, is used as an immunomodulatory and antiinflammatory agent for the management of autoimmune and rheumatic diseases such as systemic lupus erythematosus. Lately, there has been interest in its potential efficacy against severe acute respiratory syndrome coronavirus 2, with several speculated mechanisms. The purpose of this review is to elaborate on the mechanisms surrounding hydroxychloroquine. The review is an in-depth analysis of the antimalarial, immunomodulatory, and antiviral mechanisms of hydroxychloroquine, with detailed and novel pictorial explanations. The mechanisms of hydroxychloroquine are related to potential cardiotoxic manifestations and demonstrate potential adverse effects when used for coronavirus disease 2019 (COVID-19). Finally, current literature associated with hydroxychloroquine and COVID-19 has been analyzed to interrelate the mechanisms, adverse effects, and use of hydroxychloroquine in the current pandemic. Currently, there is insufficient evidence about the efficacy and safety of hydroxychloroquine in COVID-19. KEY MESSAGES 1. HCQ, initially an antimalarial agent, is used as an immunomodulatory agent for managing several autoimmune diseases, for which its efficacy is linked to inhibiting lysosomal antigen processing, MHC-II antigen presentation, and TLR functions. 2. HCQ is generally well-tolerated although severe life-threatening adverse effects including cardiomyopathy and conduction defects have been reported. 3. HCQ use in COVID-19 should be discouraged outside clinical trials under strict medical supervision.

Background Coronavirus disease 2019 (COVID-19) has been reported to cause worse outcomes in patients with underlying cardiovascular disease, especially in patients with acute cardiac injury, which is determined by elevated levels of high-sensitivity troponin. There is a paucity of data on the impact of congestive heart failure (CHF) on outcomes in COVID-19 patients. Methods We conducted a literature search of PubMed/Medline, EMBASE, and Google Scholar databases from 11/1/2019 till 06/07/2020, and identified all relevant studies reporting cardiovascular comorbidities, cardiac biomarkers, disease severity, and survival. Pooled data from the selected studies was used for metanalysis to identify the impact of risk factors and cardiac biomarker elevation on disease severity and/or mortality. Results We collected pooled data on 5,967 COVID-19 patients from 20 individual studies. We found that both non-survivors and those with severe disease had an increased risk of acute cardiac injury and cardiac arrhythmias, our pooled relative risk (RR) was — 8.52 (95% CI 3.63–19.98) (p<0.001); and 3.61 (95% CI 2.03–6.43) (p=0.001), respectively. Mean difference in the levels of Troponin-I, CK-MB, and NT-proBNP was higher in deceased and severely infected patients. The RR of in-hospital mortality was 2.35 (95% CI 1.18–4.70) (p=0.022) and 1.52 (95% CI 1.12–2.05) (p=0.008) among patients who had pre-existing CHF and hypertension, respectively. Conclusion Cardiac involvement in COVID-19 infection appears to significantly adversely impact patient prognosis and survival. Pre-existence of CHF, and high cardiac biomarkers like NT-pro BNP and CK-MB levels in COVID-19 patients correlates with worse outcomes.

Objective Aim of the study was to examine the effects of the vitamin D (Vit-D) treatment and non-treatment on Vit-D-deficient patients without a prior history of myocardial infarction (MI). Materials and Methods This is an retrospective, observational, nested case-control study of patients (N=20,025) with low 25-hydroxyvitamin D [(25-OH)D] levels (&lt;20 ng/ml) who received care at the Veterans Health Administration from 1999-2018. Patients were divided into three groups: Group A (untreated, levels ≤20 ng/ml), Group B (treated, levels 21-29 ng/ml), and Group C (treated, levels ≥30 ng/ml). The risk of MI and all-cause-mortality were compared utilizing propensity score-weighted cox-proportional hazard models. Results Among the cohort of 20,025 patients, the risk of MI was significantly lower in Group C, compared to Group B [hazard ratio (HR) 0.65, 95% CI; 0.49-0.85, P=.002] and Group A (HR 0.73, 95% CI; 0.55-0.96), P=.02). There was no difference in the risk of MI between Group B and Group A (HR 1.14, 95% CI; 0.91-1.42, P=.24]. Compared to Group A, both Group B (HR 0.59, 95% CI; 0.54-0.63, P&lt;.001] and Group C (HR 0.61, 95% CI; 0.56-0.67, P&lt;.001] had significantly lower all-cause-mortality. There was no difference in all-cause-mortality between Group B and Group C (HR 0.99, 95% CI; 0.89-1.09, P=.78). Conclusions In patients with Vit-D-deficiency and no prior history of MI, treatment to the (25-OH)D level of &gt;20 ng/ml and &gt;30 ng/ml was associated with a significantly lower risk of all-cause-mortality. The lower risk of MI was observed only in individuals maintaining the (25-OH)D levels ≥30 ng/ml.

Background Left ventricular thrombus (LVT) is not uncommon and pose a risk of systemic embolism, which can be mitigated by adequate anticoagulation. Direct oral anticoagulants (DOACs) are increasingly being used as alternatives to warfarin for anticoagulation, but their efficacy and safety profile has been debated. We aim to compare the therapeutic efficacy and safety of DOACs versus warfarin for the treatment of LVT. Methodology We systematically searched PubMed/Medline, Google Scholar, Cochrane library, and LILCAS databases from inception to 14th August 2020 to identify relevant studies comparing warfarin and DOACs for LVT treatment and used the pooled data extracted from retrieved studies to perform a meta-analysis. Results We report pooled data on 1955 patients from 8 studies, with a mean age of 61 years and 59.7 years in warfarin and DOACs group, respectively. The pooled odds ratio for thrombus resolution was 1.11 (95% CI 0.51–2.39) on comparing warfarin to DOAC, but it did not reach a statistical significance (p = 0.76). The pooled risk ratio (RR) of stroke or systemic embolization and bleeding in patients treated with warfarin vs DOACs was 1.04 (95% CI 0.64–1.68; p = 0.85), and 1.15 (95% CI 0.62–2.13; p = 0.57), respectively; with an overall RR of 1.09 (95% CI 0.70–1.70; p = 0.48) for mortality. Conclusions DOACs appears to be non-inferior or at least as effective as warfarin in the treatment of left ventricular thrombus without any statistical difference in stroke or bleeding complications.